Experimental studies support the link between such metabolic disturbances and AD with impaired amyloid or tau pathologies being worsened following the development of obesity and insulin-resistance in transgenic AD models of amyloidogenesis or Tau pathology (Ho et al., 2004; Julien et al., 2010; Kohjima et al., 2010; Takeda et al., 2010; Leboucher et al., 2013; Moser and Pike, 2017). The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.